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nature portfolio permissions reprints privacy policy accession numbers gse43956 advertising gene expression responses social media glucocorticoid-inducible protein kinase high-salt diet develop nature med nature genet glucocorticoid-inducible kinase isoforms regulating il-23r expression nature immunol salt-sensitive hypertension monica glucocorticoid-inducible kinase sgk1 regulate th17 development nature 479 nature 496 nature integrin-mediated cell adhesion promotes il-23r expression content rubbing salt itk independent development springerlink instant access enhancing th17-mediated immunity regulates adipocyte differentiation glucocorticoid-inducible kinase 1 sgk1–/– data sets microarray data sets immune responses shannon permissions microarray data analysis il-23r expression h3k27me3 reveals specificity salt induces murine high salt memory high salt intake th17 responses promotes tissue inflammation th17 cell specification enhance th17 differentiation privacy personal data trigger tissue inflammation govern na+ transport pathogenic th17 cells th17 cell phenotype gse43957 gse43969

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         headline:Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1
         description:Transcriptional profiling of developing TH17 cells identifies serum glucocorticoid kinase 1 (SGK1) as an essential node downstream of IL-23 signalling, and transcriptional analysis shows that a modest increase in salt concentration induces SGK1 expression, promotes IL-23 receptor expression and enhances TH17 cell differentiation, accelerating the development of autoimmunity. Two independent groups have come to the same surprising conclusion: that increased salt concentrations promote autoimmune disease by stimulating the production of interleukin-17-producing helper T (TH17) cells from CD4+ T cells. Chuan Wu et al. show that increases in salt concentrations induce serum glucocorticoid kinase 1 (SGK1) in T cells and enhance TH17 differentiation in vitro and in vivo in mice. Markus Kleinewietfeld et al. find that salt induces murine and human TH17 cells by a mechanism dependent on activation of SGK1 and the p38 MAP kinase/NFAT5 pathway. Mice on a high-salt diet develop a more severe experimental autoimmune encephalomyelitis, a model for brain inflammation, owing to high numbers of infiltrating TH17 cells. These studies raise the possibility that high salt intake might trigger tissue inflammation and autoimmune disease in humans. A further paper from Nir Yosef et al. presents a global view of the gene networks regulating TH17 cell differentiation. TH17 cells (interleukin-17 (IL-17)-producing helper T cells) are highly proinflammatory cells that are critical for clearing extracellular pathogens and for inducing multiple autoimmune diseases1. IL-23 has a critical role in stabilizing and reinforcing the TH17 phenotype by increasing expression of IL-23 receptor (IL-23R) and endowing TH17 cells with pathogenic effector functions2,3. However, the precise molecular mechanism by which IL-23 sustains the TH17 response and induces pathogenic effector functions has not been elucidated. Here we used transcriptional profiling of developing TH17 cells to construct a model of their signalling network and nominate major nodes that regulate TH17 development. We identified serum glucocorticoid kinase 1 (SGK1), a serine/threonine kinase4, as an essential node downstream of IL-23 signalling. SGK1 is critical for regulating IL-23R expression and stabilizing the TH17 cell phenotype by deactivation of mouse Foxo1, a direct repressor of IL-23R expression. SGK1 has been shown to govern Na+ transport and salt (NaCl) homeostasis in other cells5,6,7,8. We show here that a modest increase in salt concentration induces SGK1 expression, promotes IL-23R expression and enhances TH17 cell differentiation in vitro and in vivo, accelerating the development of autoimmunity. Loss of SGK1 abrogated Na+-mediated TH17 differentiation in an IL-23-dependent manner. These data demonstrate that SGK1 has a critical role in the induction of pathogenic TH17 cells and provide a molecular insight into a mechanism by which an environmental factor such as a high salt diet triggers TH17 development and promotes tissue inflammation.
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      description:Transcriptional profiling of developing TH17 cells identifies serum glucocorticoid kinase 1 (SGK1) as an essential node downstream of IL-23 signalling, and transcriptional analysis shows that a modest increase in salt concentration induces SGK1 expression, promotes IL-23 receptor expression and enhances TH17 cell differentiation, accelerating the development of autoimmunity. Two independent groups have come to the same surprising conclusion: that increased salt concentrations promote autoimmune disease by stimulating the production of interleukin-17-producing helper T (TH17) cells from CD4+ T cells. Chuan Wu et al. show that increases in salt concentrations induce serum glucocorticoid kinase 1 (SGK1) in T cells and enhance TH17 differentiation in vitro and in vivo in mice. Markus Kleinewietfeld et al. find that salt induces murine and human TH17 cells by a mechanism dependent on activation of SGK1 and the p38 MAP kinase/NFAT5 pathway. Mice on a high-salt diet develop a more severe experimental autoimmune encephalomyelitis, a model for brain inflammation, owing to high numbers of infiltrating TH17 cells. These studies raise the possibility that high salt intake might trigger tissue inflammation and autoimmune disease in humans. A further paper from Nir Yosef et al. presents a global view of the gene networks regulating TH17 cell differentiation. TH17 cells (interleukin-17 (IL-17)-producing helper T cells) are highly proinflammatory cells that are critical for clearing extracellular pathogens and for inducing multiple autoimmune diseases1. IL-23 has a critical role in stabilizing and reinforcing the TH17 phenotype by increasing expression of IL-23 receptor (IL-23R) and endowing TH17 cells with pathogenic effector functions2,3. However, the precise molecular mechanism by which IL-23 sustains the TH17 response and induces pathogenic effector functions has not been elucidated. Here we used transcriptional profiling of developing TH17 cells to construct a model of their signalling network and nominate major nodes that regulate TH17 development. We identified serum glucocorticoid kinase 1 (SGK1), a serine/threonine kinase4, as an essential node downstream of IL-23 signalling. SGK1 is critical for regulating IL-23R expression and stabilizing the TH17 cell phenotype by deactivation of mouse Foxo1, a direct repressor of IL-23R expression. SGK1 has been shown to govern Na+ transport and salt (NaCl) homeostasis in other cells5,6,7,8. We show here that a modest increase in salt concentration induces SGK1 expression, promotes IL-23R expression and enhances TH17 cell differentiation in vitro and in vivo, accelerating the development of autoimmunity. Loss of SGK1 abrogated Na+-mediated TH17 differentiation in an IL-23-dependent manner. These data demonstrate that SGK1 has a critical role in the induction of pathogenic TH17 cells and provide a molecular insight into a mechanism by which an environmental factor such as a high salt diet triggers TH17 development and promotes tissue inflammation.
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